Objective To investigate the association between the TyG index,its modified variants,and the risk of developing colorectal cancer(CRC).Methods This study included a total of 93,177 participants from the 2006 Kailuan Group health examination cohort.Participants were categorized into four quartiles(Q1-Q4)according to their TyG and modified TyG indices.Follow-up began at the baseline examination,with incident CRC as the primary outcome.Participants were censored at the time of CRC diagnosis,death,or the end of the study,whichever occurred first.The dose-response relationship between TyG and its modified indices and the risk of CRC was evalu-ated using restricted cubic splines(RCS)in conjunction with Cox proportional hazards regression models,yielding hazard ratios(HRs)and 95%confidence intervals(CIs).To compare the strength of associations between TyG and its modified versions(TyG-BMI,TyG-WC,TyG-WHR,TyG-WHtR,TyG-WWI)and CRC risk,HRs for CRC per one standard deviation increase in each index were calculated and compared.Results Both the TyG index and its modified variants demonstrated a significant dose-response relationship with the risk of CRC incidence.Specifically,for the TyG index,each 1-standard deviation(SD)increase was associated with a 1.17-fold(95%CI:1.09～1.27)higher risk of CRC.Compared with the first quartile(Q1),the third quartile(Q3)and fourth quartile(Q4)exhibited a 1.25-fold(95%CI:1.01～1.55)and 1.26-fold(95%CI:1.01～1.57)increased risk,respectively.For TyG-BMI,each 1-SD increase was linked to a 1.20-fold(95%CI:1.07～1.35)elevated CRC risk.Compared with Q1,Q3 and Q4 showed a 1.32-fold(95%CI:1.06～1.64)and 1.51-fold(95%CI:1.21～1.88)increase,respectively.Regarding TyG-WC,each 1-SD increment was associated with a 1.22-fold(95%CI:1.13～1.32)higher CRC risk,with Q3 and Q4 showing a 1.35-fold(95%CI:1.08～1.70)and 1.56-fold(95%CI:1.24～1.96)increased risk compared to Q1.For TyG-WHtR,each 1-SD increase was associated with a 1.24-fold(95%CI:1.08-1.42)higher CRC risk.Compared with Q1,Q2,Q3,and Q4 demonstrated a 1.31-fold(95%CI:1.03～1.66),1.55-fold(95%CI:1.23～1.95),and 1.60-fold(95%CI:1.27～2.02)increase,respectively.In the case of TyG-WHR,each 1-SD increase was associated with a 1.19-fold(95%CI:1.10～1.29)higher CRC risk,with Q4 showing a 1.42-fold(95%CI:1.14～1.77)increased risk compared to Q1.Finally,for TyG-WWI,each 1-SD increase was associated with a 1.22-fold(95%CI:1.13～1.32)elevated CRC risk,with both Q3 and Q4 showing a 1.58-fold increase(Q3:95%CI:1.26～1.98;Q4:95%CI:1.25～1.99).Stratified analyses by sex and age consistently revealed significant associations between the TyG index and its modified variants and CRC risk.Furthermore,these indices were independently associated with the incidence of both colon cancer and rectal cancer.Conclusions(1)Elevated levels of the TyG index and its modified variants are independent risk factors for CRC.(2)Both the TyG index and its modified forms demonstrate a significant dose-response association with the incidence of CRC.(3)Among the modified TyG indices,TyG-WWI,TyG-WHtR,TyG-BMI,TyG-WC,and TyG-WHR showed stronger correlations with CRC risk compared to the original TyG index.

Objective To investigate the association between the TyG index,its modified variants,and the risk of developing colorectal cancer(CRC).Methods This study included a total of 93,177 participants from the 2006 Kailuan Group health examination cohort.Participants were categorized into four quartiles(Q1-Q4)according to their TyG and modified TyG indices.Follow-up began at the baseline examination,with incident CRC as the primary outcome.Participants were censored at the time of CRC diagnosis,death,or the end of the study,whichever occurred first.The dose-response relationship between TyG and its modified indices and the risk of CRC was evalu-ated using restricted cubic splines(RCS)in conjunction with Cox proportional hazards regression models,yielding hazard ratios(HRs)and 95%confidence intervals(CIs).To compare the strength of associations between TyG and its modified versions(TyG-BMI,TyG-WC,TyG-WHR,TyG-WHtR,TyG-WWI)and CRC risk,HRs for CRC per one standard deviation increase in each index were calculated and compared.Results Both the TyG index and its modified variants demonstrated a significant dose-response relationship with the risk of CRC incidence.Specifically,for the TyG index,each 1-standard deviation(SD)increase was associated with a 1.17-fold(95%CI:1.09～1.27)higher risk of CRC.Compared with the first quartile(Q1),the third quartile(Q3)and fourth quartile(Q4)exhibited a 1.25-fold(95%CI:1.01～1.55)and 1.26-fold(95%CI:1.01～1.57)increased risk,respectively.For TyG-BMI,each 1-SD increase was linked to a 1.20-fold(95%CI:1.07～1.35)elevated CRC risk.Compared with Q1,Q3 and Q4 showed a 1.32-fold(95%CI:1.06～1.64)and 1.51-fold(95%CI:1.21～1.88)increase,respectively.Regarding TyG-WC,each 1-SD increment was associated with a 1.22-fold(95%CI:1.13～1.32)higher CRC risk,with Q3 and Q4 showing a 1.35-fold(95%CI:1.08～1.70)and 1.56-fold(95%CI:1.24～1.96)increased risk compared to Q1.For TyG-WHtR,each 1-SD increase was associated with a 1.24-fold(95%CI:1.08-1.42)higher CRC risk.Compared with Q1,Q2,Q3,and Q4 demonstrated a 1.31-fold(95%CI:1.03～1.66),1.55-fold(95%CI:1.23～1.95),and 1.60-fold(95%CI:1.27～2.02)increase,respectively.In the case of TyG-WHR,each 1-SD increase was associated with a 1.19-fold(95%CI:1.10～1.29)higher CRC risk,with Q4 showing a 1.42-fold(95%CI:1.14～1.77)increased risk compared to Q1.Finally,for TyG-WWI,each 1-SD increase was associated with a 1.22-fold(95%CI:1.13～1.32)elevated CRC risk,with both Q3 and Q4 showing a 1.58-fold increase(Q3:95%CI:1.26～1.98;Q4:95%CI:1.25～1.99).Stratified analyses by sex and age consistently revealed significant associations between the TyG index and its modified variants and CRC risk.Furthermore,these indices were independently associated with the incidence of both colon cancer and rectal cancer.Conclusions(1)Elevated levels of the TyG index and its modified variants are independent risk factors for CRC.(2)Both the TyG index and its modified forms demonstrate a significant dose-response association with the incidence of CRC.(3)Among the modified TyG indices,TyG-WWI,TyG-WHtR,TyG-BMI,TyG-WC,and TyG-WHR showed stronger correlations with CRC risk compared to the original TyG index.

Liver cancer is one of the most threatening diseases to the human body,and most patients are already in the advanced stage at the time of diagnosis,resulting in an extremely high mortality rate.The diagnosis and treatment of early-stage liver cancer is the key to improving the prognosis of patients.Medical imaging is an important method that assists in the diagnosis of liver cancer,and currently,intelligent image recognition technology based on medical imaging data has been widely applied in the field of medical diagnosis and has good application prospects.This article reviews the current status of research on artificial intelligence(AI)methods for the diagnosis of focal liver lesions based on liver medical images and proposes the advantages and shortcomings of current AI diagnosis,so as to provide new research ideas for the intelligent diagnosis of liver cancer in the future.

Objective:To evaluate the safety and efficacy of tumor-treating fields (TTFields) and chemoradiation in patients with high-grade glioblastoma.Methods:Clinical data of 38 patients admitted to the Jiangsu Cancer Hospital from September 2021 to May 2023 who were diagnosed with high-grade glioblastoma (36 cases of World Health Organization grade Ⅳ and 2 cases of grade Ⅲ) were retrospectively analyzed. All patients received TTFields combined with concurrent chemoradiation after surgery. Response assessment in neuro-oncology (RANO) criteria was used to evaluate the glioma responses as tumor remission, stable or progression. Common terminology criteria for adverse events v5.0 and TTFields related skin adverse reaction (dAE) criteria were used to evaluate the adverse events. Treatment compliance was assessed by data on the NovoTTF-200A therapeutic device, calculated as a percentage of daily TTFields usage time. Survival analysis was estimated by the Kaplan-Meier method and compared by the log-rank test.Results:The median duration of treatment with TTFields in 38 patients was 20 h (rang: 2.4-22.6 h), and the median treatment compliance was 83% (range: 10%-94%). After 42 days of TTFields combined with concurrent chemoradiation, 12 patients who underwent complete tumor resection were assessed as stable according to RANO criteria. Among the 26 patients who underwent partial tumor resection, 23 (88%) were evaluated as disease remission according to RANO criteria. The 7-, 10-, 13-month progression-free survival rate was 81.0%、64.0%、49.5%, repectively. The common adverse events included grade 1 (45%) and grade 2 (8%) dAE, without grade 3-4 dAE. Typical presentations included contact dermatitis, blisters, lesions or ulcers, and abscesses. The median follow-up time was 10.0 months (range: 1.6-21.3 months). At follow-up as of July 2023, 26 of the 38 patients were stable and 12 had disease progression (8 died).Conclusion:The preliminary results show that TTFields combined with chemoradiation is effective, safe and reliable treatment for high-grade glioblastoma.

Objective To investigate the core drugs of traditional Chinese medicine(TCM)for the treatment of hypoxic pulmonary hypertension(HPH),and to verify the drug efficacy by hypoxia combined with Su5416(Hypoxia+Su5416,HySu)-induced PH mouse model.Methods Relevant literatures on TCM treatment of HPH in China Knowledge Network,Wanfang,Weipu were collected,screened and set up a database through the nerf criteria,and inputted into the software of traditional Chinese medicine inheritance assistance platform(V2.5)for the excavation of medication law.The HySu-PH mouse model was established,and the core drugs were evaluated for drug efficacy through force exhaustion exercise running table,blood oxygen saturation,right ventricular pressure,and right heart hypertrophy index test.Results The 102 relevant formulas for the treatment of HPH were screened,involving a total of 158 traditional Chinese medicines,and the top 5 drug frequencies were Salvia miltiorrhiza,Rhizoma Chuanxiong,Astragalus membranaceus,Draba hebecarpa,and Angelica sinensis,with the highest use of blood-activating and blood-stasis removing drugs,and deficiency-tonifying drugs in the categories of drugs used,and Salvia miltiorrhiza was the core drug used.HySu-PH mouse models were constructed and given 2 weeks of treatment with the danshen preparation Danshen injection.Danshen injection significantly elevated body weight(P<0.01),oxygen saturation(P<0.05),displacement of exhaustion(P<0.01),and duration of exhaustion(P<0.05),and lowered the right ventricular systolic blood pressure(P<0.01)and the right cardiac hypertrophy index(P<0.01).Conclusion Salvia miltiorrhiza is a core drug for the treatment of HPH,and the danshen preparation Danshen injection can effectively treat HySu-PH.

Objective To investigate the therapeutic effects of Xingzhi Yinao (XZYN) particles combined with hyperbaric oxygen therapy on cognitive impairment and motor dysfunction in patients with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods Sixty-seven patients with DEACMP were admitted to the Affiliated Yantai Yuhuangding Hospital of Qingdao University from January 2011 to December 2015, and they were randomly divided into a control group (given conventional treatment such as inhalation of oxygen, cytidine diphosphate cholin and vitamin B, 19 cases), a hyperbaric oxygen (HBO) treatment group (given conventional treatment + hyperbaric oxygen therapy once a day, 24 cases) and a XZYN particles treatment (XZYN group, given conventional treatment, hyperbaric oxygen and XZYN particles, 24 cases), the therapeutic course being 2 months in the three groups. Before and after treatment for 1 and 2 months, the cognitive function and motor function of the patients were evaluated by the use of activity of daily living (ADL) scale, Montreal cognitive assessment (MoCA) scale, and mini-mental state examination (MMSE) scale; the severity of cerebral white matter injury was assessed by age related white matter changes (ARWMC) scale; and the electromyographic evoked potential was used to detect the amplitude and latency of P300 to assess the severity of cognition impairment and prognosis. Results With the prolongation of therapeutic time, after treatment, the neurological function scores of ADL, MoCA, MMSE and amplitude of P300 were increased, while ARWMC was decreased and the latency of P300 was shortened gradually in the three groups, and the changes of above indexes after treatment for 2 months in XZYN group were more significant than those in either HBO group or control group[ADL score: 70.2±8.3 vs. 60.5±8.1, 23.0±6.1, MoCA score: 26.1±3.1 vs. 22.2±2.7, 18.2±3.6, MMSE score:25.9±4.1 vs. 22.4±3.5, 18.1±4.5, ARWMC score: 7.0±2.1 vs. 8.7±2.2, 15.2±3.3, latency of P300 (ms):332.9±20.4 vs. 352.5±23.6, 381.7±30.3, amplitude of P300 (μV): 6.5±1.6 vs. 5.6±1.3, 4.1±1.5, all P < 0.05]. Conclusion The hyperbaric oxygen therapy combined with XZYN particles for treatment of patients with DEACMP can significantly improve their cognitive and motor functions and ameliorate the severity of cerebral white matter injury.

Objective To explore the effects of N-butylphthalide on the expressions of ZO-1 and claudin-5 in blood-brain barrier (BBB) in rats with acute carbon monoxide (CO) poisoning. Methods A total of 144 adult healthy male Sprague-Dawley (SD) rats were randomly divided into normal control group, CO poisoning group, and NBP treatment group, with 48 rats in each group. The acute CO poisoning model was reproduced in hyperbaric oxygen chamber, and all model rats were given hyperbaric oxygen therapy once daily. The rats in the normal control group were free to breathe fresh air. The rats in NBP treatment group were administered orally NBP 60 mg/kg twice a day at 2 hours after poisoning until death. The rats in normal control group and CO poisoning group were treated with equal amount of pure olive oil. Four rats were sacrificed from each group at 1, 3, 7, 14 days after model reproducing, respectively. The changes in ultrastructure of BBB were observed under transmission electron microscope. The expressions of ZO-1 and claudin-5 proteins were determined by immunofluorescence staining and Western Blot. The localization of the two target proteins was observed by immunofluorescence double staining. The correlation between the two proteins was analyzed by linear regression. Results The ultrastructure of BBB was normal in normal control group, some ZO-1 and a large number of claudin-5 positive cells were observed. The ultrastructure of BBB was seriously injured, ZO-1 and claudin-5 positive cells in brain tissue were significantly decreased, and the expressions of ZO-1 and claudin-5 proteins in brain tissue at 1 day after poisoning in CO poisoning group were significantly lower than those of normal control group (ZO-1 protein:3.38±0.30 vs. 24.50±5.62, claudin-5 protein: 11.38±0.93 vs. 46.35±6.88, both P < 0.05), and although gradually restored, they were maintained at relatively lower levels until 14 days as compared with those in normal control group (ZO-1 protein: 10.35±0.80 vs. 24.63±3.57, claudin-5 protein: 32.35±3.11 vs. 46.43±7.20, both P < 0.05). NBP treatment could significantly alleviate the ultrastructure injury of BBB induced by acute CO poisoning, the amount of ZO-1 and claudin-5 positive cells in brain tissue were significantly increased, as well as the expressions of ZO-1 and claudin-5 proteins were significantly increased, which were significantly higher than those of CO poisoning group from 1 day and 3 days on, respectively (1-day ZO-1 protein: 7.57±0.69 vs. 3.38±0.30, 3-day claudin-5 protein:20.46±1.42 vs. 11.43±0.86, both P < 0.05), and which showed an increase tendency with time prolongation. The results of immunofluorescence double staining showed that ZO-1 and claudin-5 proteins could not only coexist in the same cell, but also could be expressed separately in different cells. Linear regression analysis showed the positive correlation between the expressions of ZO-1 and claudin-5 proteins in brain tissue of rats with acute CO poisoning (R2= 0.917, P = 0.022). Conclusion NBP could markedly improve the ultrastructure and functional integrity of BBB through up-regulating the expressions of ZO-1 and claudin-5 proteins, and then reduce brain damage caused by CO poisoning.

Objective To explore the neuroprotective effect of targeted regulation Nrf2 gene on rats with brain injury caused by acute severe carbon monoxide ( CO ) poisoning. Methods A total of 180 healthy adult SD rats were divided into 4 groups at random:normal control group( NC group) ,CO poisoning group(CO group),lentivirus group(LV group) and Nrf2 gene therapy group(Nrf2 group),and 45 rats in each group. An acute CO toxic rat model was established by inhalation in a hyperbaric oxygen tank. The lentivirus group was directly injected with lentivirus dilution (4×106 TU/μl) into striatum with a microsy-ringe guided by a stereotactic apparatus,and the Nrf2 gene therapy group was administrated the same dose of recombinant Nrf2 gene lentivirus dilution,while rats in the normal control group and the CO poisoning group were received the same amount of normal saline. Five rats were taken and decapitated at day 1,day 7 and week 2 from each group,respectively. The mitochondrial membrane potential (MMP) of neurons in brain tis-sue was detected by JC-1 method,and the expressions of Nrf2 and GCLC proteins were observed by immuno-histochemistry and Western Blot. Results Compared with the NC group (cortex:(75. 3±6. 8);hippocam-pus:(76. 4±7. 1);striatum:(73. 8±7. 3)) at the same time point,the MMPs of neurons in CO group (cor-tex:(34. 5±6. 7);hippocampus:(30. 3±5. 6);striatum:(41. 5±6. 1) and LV group (cortex:(36. 8±6. 2);hippocampus:(30. 8±6. 0);striatum:(42. 7±6. 3)) were significantly decreased,and the difference was sig-nificant(P<0. 05). However,there was no significant difference between the CO poisoning group and the lentivirus group (P>0. 05). A small amount of Nrf2 protein (0. 22±0. 05) and GCLC protein (0. 24±0. 04) were expressed in the brain tissue of normal control rats. The expressions of Nrf2 protein (0. 31±0. 06,0. 31 ±0. 05) and GCLC protein (0. 30±0. 04,0. 31±0. 07) in CO group and LV group were slightly increased (P<0. 05). Similarly,there was no significant difference between the CO poisoning group and the lentivirus group (P>0. 05). The MMPs value of nerve cells in the Nrf2 group (cortex:(53. 3±5. 3);hippocampus:(56. 9±6. 1);striatum:(60. 6±6. 0)) also decreased,but it was significantly higher than that in the CO group and the LV group at the same time point (P<0. 05) . The expression of Nrf2 in brain tissue was signifi-cantly increased (0. 59±0. 05),and there was significant difference between CO group and LV group at the same time point (P<0. 05);GCLC protein increased slightly (0. 37±0. 06),but there was no statistical difference compared with CO poisoning group and lentivirus group (P>0. 05). Conclusion CO poisoning could induce oxidative stress and damage mitochondrial function of nerve cells. The active state of targeted regulation Nrf2 could significantly enhance the antioxidant capacity of rats and positively protect rats against brain injury induced by acute severe CO poisoning.

Objective To explore the mechanism of ultrastructural and functional impairment of mitochondria and the protective effect of sulforaphane (SFP) at different dosages on hippocampus neurons in rats after acute carbon monoxide(CO)poisoning.Methods One hundred and fifty adult healthy SD rats were randomly divided into the normal control group,the CO poisoning group and the SFP treatment group.The rat model of CO poisoning was established through exposure to CO in a hyperbaric chamber.The uhrastructural changes of mitochondria in nerve cells of the brain tissue were observed by transmission electron microscopy (TEM).Mitochondrial membrane potential (MFI) was detected with JC-1 fluorescent probe,and the expressions of Nrf-2 and Trx-1 proteins and mRNA were evaluated by immunohistochemistry and quantitative RT-PCR before and after intervention.Results CO poisoning could induce impairment of mitochondria ultrastructure in neurocytes in the brain tissue.SFP could obviously alleviate the damage of mitochondria ultrastructure.The MFI level in the brain tissue was obviously reduced in rats after CO exposure.Though MFI level was decreased 3 to 7 days after SFP administration,its level was significantly higher than that of the CO poisoning group at the same time point (P ＜0.05).As compared with those in the normal control group,the expression levels of Nrf-2 and Trx-1 proteins as well as their mRNA in the CO poisoning group were slightly increased (P ＜ 0.05).After treatment with SFP,the expressions of both the proteins and mRNA were obviously increased,and there was significant difference when compared with that of the CO poisoning group at the same time point (P ＜0.05).Conclusion Early administration of either moderate or high dose SFP could efficiently improve mitochondrial structure and function,enhance anti-oxidative stress of cells,thus exerting a positive effect against brain damage induced by acute CO poisoning.

Objective To explore the mechanism of ultrastructural and functional impairment of mitochondria and the protective effect of sulforaphane (SFP) at different dosages on hippocampus neurons in rats after acute carbon monoxide(CO)poisoning.Methods One hundred and fifty adult healthy SD rats were randomly divided into the normal control group,the CO poisoning group and the SFP treatment group.The rat model of CO poisoning was established through exposure to CO in a hyperbaric chamber.The uhrastructural changes of mitochondria in nerve cells of the brain tissue were observed by transmission electron microscopy (TEM).Mitochondrial membrane potential (MFI) was detected with JC-1 fluorescent probe,and the expressions of Nrf-2 and Trx-1 proteins and mRNA were evaluated by immunohistochemistry and quantitative RT-PCR before and after intervention.Results CO poisoning could induce impairment of mitochondria ultrastructure in neurocytes in the brain tissue.SFP could obviously alleviate the damage of mitochondria ultrastructure.The MFI level in the brain tissue was obviously reduced in rats after CO exposure.Though MFI level was decreased 3 to 7 days after SFP administration,its level was significantly higher than that of the CO poisoning group at the same time point (P ＜0.05).As compared with those in the normal control group,the expression levels of Nrf-2 and Trx-1 proteins as well as their mRNA in the CO poisoning group were slightly increased (P ＜ 0.05).After treatment with SFP,the expressions of both the proteins and mRNA were obviously increased,and there was significant difference when compared with that of the CO poisoning group at the same time point (P ＜0.05).Conclusion Early administration of either moderate or high dose SFP could efficiently improve mitochondrial structure and function,enhance anti-oxidative stress of cells,thus exerting a positive effect against brain damage induced by acute CO poisoning.